Hypertension is a condition characterized by prolonged periods of high blood pressure. Hypertension can lead to an enlarged or damaged heart (hypertrophy) and, eventually, heart failure. Though treatable, hypertension is the primary cause of death for tens of thousands of patients per year in the United States. Hypertension is also listed as a primary or contributing cause of death for hundreds of thousands of patients per year in the United States and affects an estimated 65 million people in the United Sates alone. Therefore, hypertension is a serious health problem necessitating significant research and development of effective treatment.
Blood pressure typically becomes elevated when resistance to blood flow increases. Increased resistance to blood flow can be caused by a variety of factors, including constriction of blood vessels and excessive fluid in the blood. For example, when blood vessels constrict due to plaque build-up on the lining of arterial walls, additional force is required to pump the same volume of blood through the blood vessels. Similarly, when fluid levels in the blood stream increase, additional force is required to pump blood throughout the body to meet the body's needs. The additional force required to maintain a sufficient volumetric flow rate of blood within a constricted space or in a diluted media increases blood pressure.
The body can generally tolerate short periods of increased blood pressure by activating a temporary autonomic response that causes blood pressure to decline. Specifically, the body's autonomic response inhibits the sympathetic nervous system and activates the parasympathetic nervous system. In inhibiting the sympathetic nervous system, the brain directs the heart to decrease cardiac output, the kidneys to reduce blood volume by expunging sodium and water, and the arterioles to dilate. In activating the parasympathetic nervous system, the brain relaxes the body's muscles, decreases the rate of respiration, and signals the heart to reduce the frequency of contractions. These physiologic changes can temporarily decrease blood pressure.
When blood pressure becomes elevated, the body's autonomic response is triggered by stretch-sensitive mechanoreceptors, or baroreceptors, located in the walls of the heart and various major blood vessels. Rising blood pressure forces blood vessels to expand. This, in turn, causes baroreceptors located in vascular walls to become distended. As baroreceptors become distended, they generate action potentials more frequently, signaling the brain to activate an autonomic response called the baroreflex that counteracts the increase in pressure. In this manner, baroreceptors relay signals to the brain related to changes in blood pressure.
To improve upon carotid sinus nerve stimulation, a new device and method for treating hypertension and heart failure has been introduced. The Rheos® system and the method is called Baroreflex Activation Therapy™ (or BAT™) for direct stimulation of baroreceptors, or vessels that contain baroreceptors. The CVRx BAT system has proven in clinical trials to effectively remodel cardiac structure and improve function while reducing blood pressure, thus showing efficacy for both hypertension and heart failure. U.S. Pat. No. 6,522,926 to Kieval, et al. discloses a system and method for activating baroreceptors to regulate blood pressure. By treating hypertension through BAT, a coordinated stimulation of baroreceptors produces the same physiologic response produced by baropacing while avoiding direct nerve stimulation.
However, while showing significant efficacy clinically, there are limitations to current procedures for electrical stimulation of baroreceptors or vessels that contain baroreceptors, the first limitation being the relative invasiveness of implanting electrodes in a patient. For patients requiring long-term device treatment for hypertension or other conditions, an electrical stimulation unit and one or more electrode assemblies may be implanted into a patient in a clinical setting. Incisions are made on both sides of the patients' neck to create access to the vasculature and bilateral electrodes that wrap around the carotid arteries at the level of the carotid sinus are implanted. While the safety and success of such therapies appears promising, current implantation practice typically involves dissecting free the carotid artery under general anesthesia to expose the carotid sinus in order to wrap the electrode around the artery. Although this is similar to a routine procedure performed by vascular surgeons, it carries a risk profile typically associated with surgical procedures. As expected, such procedures require the use of expensive operating facilities, staff, and equipment.
To reduce costs and potential patient risk, both fully external and less-invasive electro-stimulation techniques, have been proposed. For example, U.S. Publication 2008/0234779 discloses an external control unit providing electrical stimulation to external electrodes located on the outside of a patient's neck and to internal electrodes inserted into the patient's larynx or trachea. The system temporarily modulates certain patient parameters by electrically activating or deactivating the baroreflex during surgery.
While external activation and less-invasive techniques for electrically stimulating the baroreflex begin to address the issues of cost and patient safety, the efficiency and effectiveness of electrical stimulation may be somewhat limited in certain instances due to a lack of specificity of stimulation resulting in extraneous stimulation of tissue other than the targeted baroreceptors. An electric field applied from an electrode spreads out unequally in all directions, depending on relative conductivities of the surrounding mediums (such as blood and tissue). Consequently, it can be difficult to direct current applied from the outside of sinus bulb solely to the baroreceptors residing within the wall of the carotid sinus bulb or residing in other tissue.
Additionally, nerves exist on the surface of the carotid sinus that can cause referred pain to the patient when inadvertently stimulated. This condition is known as Carotidynia. Consequently, electrically stimulating the baroreceptors without causing incidental referred pain has been problematic in the field of baroreflex modulation.
Therefore, it would desirable to provide baroreflex modulation devices and methods that may be easily implemented externally or non-invasively and that would limit extraneous tissue stimulation.